333 0

Full metadata record

DC FieldValueLanguage
dc.contributor.author박현경-
dc.date.accessioned2016-11-03T05:32:19Z-
dc.date.available2016-11-03T05:32:19Z-
dc.date.issued2015-04-
dc.identifier.citationPEDIATRIC RESEARCH, v. 77, NO 4, Page. 554-562en_US
dc.identifier.issn0031-3998-
dc.identifier.issn1530-0447-
dc.identifier.urihttp://www.nature.com/pr/journal/v77/n4/full/pr20159a.html-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/24132-
dc.description.abstractBACKGROUND: Periventricular leukomalacia (PVL) is a major form of preterm brain injury. Na+-K+-Cl- 1 cotransporter (NKCC1) expression on neurons and astrocytes is developmentally regulated and mediates Cl- reversal potential. We hypothesized that NKCC1 is highly expressed on oligodendrocytes (OLs) and increases vulnerability to hypoxia-ischemia (HI) mediated white matter injury, and that the NKCC1 inhibitor bumetanide would be protective in a rodent PVL model. METHODS: Immunohistochemistry in Long-Evans rats and PLP-EGFP transgenic mice was used to establish cell-specific expression of NKCC1 in the immature rodent brain. HI was induced on postnatal day 6 (P6) in rats and the protective efficacy of bumetanide (0.3 mg/kg/i.p. q12h x 60 h) established. RESULTS: NKCC1 was expressed on OLs and subplate neurons through the first 2 postnatal weeks, peaking in white matter and the subplate between P3-7. Following HI, NKCC1 is expressed on OLs and neurons. Bumetanide treatment significantly attenuates myelin basic protein loss and neuronal degeneration 7 d post-HI. CONCLUSION: Presence and relative overexpression of NKCC1 in rodent cerebral cortex coincides with a period of developmental vulnerability to HI white matter injury in the immature prenatal brain. The protective efficacy of bumetanide in this model of preterm brain injury suggests that Cl- transport is a factor in PVL and that its inhibition may have clinical application in premature human infants.en_US
dc.description.sponsorshipThis work was supported by the US National Institute of Neurological Disorders and Stroke at the National Institutes of Health (NS031718 and DP1 OD003347 from the Office of the Director to F.E.J.), the Heart and Stroke Foundation of Canada (to L.L.J), the William Randolph Hearst Foundation at Harvard Medical School (to L.L.J), the University of New Mexico Department of Pediatrics (to L.L.J), and Alberta Innovates Health Solutions Canada (to L.L.J).en_US
dc.language.isoenen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.subjectNEONATAL HYPOXIA-ISCHEMIAen_US
dc.subjectFOCAL CEREBRAL-ISCHEMIAen_US
dc.subjectK+-CL-COTRANSPORTERen_US
dc.subjectBRAIN-INJURYen_US
dc.subjectMEDIATED EXCITOTOXICITYen_US
dc.subjectNA+/CA2+ EXCHANGERen_US
dc.subjectINFANTSen_US
dc.subjectDAMAGEen_US
dc.subjectOLIGODENDROCYTESen_US
dc.subjectDISEASEen_US
dc.titleChloride cotransporter NKCC1 inhibitor bumetanide protects against white matter injury in a rodent model of periventricular leukomalaciaen_US
dc.typeArticleen_US
dc.relation.no4-
dc.relation.volume77-
dc.identifier.doi10.1038/pr.2015.9-
dc.relation.page554-562-
dc.relation.journalPEDIATRIC RESEARCH-
dc.contributor.googleauthorJantzie, Lauren L.-
dc.contributor.googleauthorHu, Melody Y.-
dc.contributor.googleauthorPark, Hyun-Kyung-
dc.contributor.googleauthorJackson, Michele C.-
dc.contributor.googleauthorYu, Jenny-
dc.contributor.googleauthorMaxwell, Jessie R.-
dc.contributor.googleauthorJensen, Frances E.-
dc.relation.code2015002409-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF MEDICINE[S]-
dc.sector.departmentDEPARTMENT OF MEDICINE-
dc.identifier.pidneopark-
Appears in Collections:
COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > Articles
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE